title: Astrocytes in glaucomatous optic neuropathy.
abstract: Glaucoma, the second most prevalent cause of blindness worldwide, is a degenerative disease characterized by loss of vision due to loss of retinal ganglion cells. There is no cure for glaucoma, but early intervention with drugs and/or surgery may slow or halt loss of vision. Increased intraocular pressure (IOP), age, and genetic background are the leading risk factors for glaucoma. Our laboratory and other investigators have provided evidence that astrocytes are the cells responsible for many pathological changes in the glaucomatous optic nerve head (ONH). Over several years, in vivo and in vitro techniques characterized the changes in quiescent astrocytes that lead to the reactive phenotype in glaucoma. Reactive astrocytes alter the homeostasis and integrity of the neural and connective tissues in the ONH of human and experimental glaucoma in monkeys. During the transition of quiescent astrocytes to the reactive phenotype altered astrocyte homeostatic functions such as cell-cell communication, migration, growth factor pathway activation, and responses to oxidative stress may impact pathological changes in POAG. Our data also suggests that the creation of a non-supportive environment for the survival of RGC axons through remodeling of the ONH by reactive astrocytes leads to progression of glaucomatous optic neuropathy.
authors.affiliation: Department of Ophthalmology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA. m-hernandez-neufeld@northwestern.edu
authors.forename: M Rosario
authors.initials: MR
authors.lastname: Hernandez
authors.forename: Haixi
authors.initials: H
authors.lastname: Miao
authors.forename: Thomas
authors.initials: T
authors.lastname: Lukas
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000473:pathology / Q000502:physiology; D002448:Cell Adhesion; D002450:Cell Communication / Q000502:physiology; D002465:Cell Movement; D002478:Cells, Cultured; D018031:Connexin 43 / Q000378:metabolism; D005109:Extracellular Matrix / Q000378:metabolism; D005902:Glaucoma, Open-Angle / Q000473:pathology / Q000503:physiopathology; D006706:Homeostasis; D006801:Humans; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D009898:Optic Disk / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D009901:Optic Nerve Diseases / Q000473:pathology / Q000503:physiopathology; D018384:Oxidative Stress; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism; D012165:Retinal Ganglion Cells / Q000378:metabolism / Q000473:pathology; D015398:Signal Transduction / Q000502:physiology; D013482:Superoxide Dismutase / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000378:metabolism; D018631:ras Proteins / Q000378:metabolism; D000099156:Superoxide Dismutase 2
chemical_list: D018031:Connexin 43; D020928:Mitogen-Activated Protein Kinases; D043562:Receptors, G-Protein-Coupled; D013482:Superoxide Dismutase; D016212:Transforming Growth Factor beta; D018631:ras Proteins; D000099156:Superoxide Dismutase 2